Diagnosis and Management of Chronic Daily

Ivan Garza, M.D.,1 and Todd J. Schwedt, M.D.2

ABSTRACT

Chronic daily headache (CDH) is a descriptive term that encompasses multiple headache diagnoses and affects 4% of the general adult population. Chronic daily headache results in significant pain and suffering with substantial impact on quality of life, and enormous economic costs to society. Although most patients with primary CDH suffer from chronic or chronic tension-type headache, other primary and secondary headache disorders can also manifest as a CDH syndrome. For CDH manage- ment to succeed, secondary need to be ruled out with proper investigations when judged necessary. If the diagnosis of primary CDH is established, diagnosis of the specific CDH subtype is imperative to institute appropriate treatment. The diagnosis and manage- ment of distinct CDH entities, chronic migraine, chronic tension-type headache, new daily persistent headache, and hemicrania continua, are the primary forms of CDH and the emphasis of this review. Although, strictly speaking, medication overuse headache is a secondary form of CDH, it is also highlighted in this review given its frequent association with primary CDH.

KEYWORDS: Chronic, daily, headache, migraine, hemicrania

Chronic daily headache (CDH) is a descriptive include female sex, low socioeconomic status, unmarried, term that encompasses several different headache diag- history of head or neck trauma, and the presence of noses. Chronic daily headache affects 4% of the adult comorbid pain disorders. Modifiable risk factors for population in the United States and around the world.1–3 CDH include obesity, snoring and other sleep disorders, The vast majority of CDH patients suffer from either high caffeine intake, smoking, and overuse of abortive chronic migraine or chronic tension-type headache. headache medications.6–9 Chronic daily headache results in significant pain and Similar to all headache types, it is essential to suffering, reduction in quality of life, and enormous exclude a secondary headache as the cause of CDH. economic costs to society.4,5 Depending upon the clinical history and examination Scher has summarized the evidence from popu- findings, further diagnostic testing may or may not be This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. lation-based studies related to risk factors influencing necessary. Although a complete list of causes for secon- the incidence, prevalence, and prognosis of CDH.6 dary CDH would be exhaustive, Table 1 summarizes Major life changes (residence change, marital status, common considerations. etc.) have been associated with the onset of CDH.7 If secondary headaches are ruled out, the clinician Nonmodifiable factors that increase the risk for CDH must determine the type of primary CDH the patient

1Department of Neurology, Mayo Clinic, Rochester, Minnesota; Headache; Guest Editor, Jerry W. Swanson, M.D., F.A.C.P. 2Washington University Headache Center, Washington University Semin Neurol 2010;30:154–166. Copyright # 2010 by Thieme School of Medicine, St. Louis, Missouri. Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, Address for correspondence and reprint requests: Ivan Garza, USA. Tel: +1(212) 584-4662. M.D., Assistant Professor, Department of Neurology, Mayo Clinic, DOI: http://dx.doi.org/10.1055/s-0030-1249224. 200 First Street SW, Rochester, MN 55905 (e-mail: garza.ivan@mayo. ISSN 0271-8235. edu). 154 DIAGNOSIS AND MANAGEMENT OF CHRONIC DAILY HEADACHE/GARZA, SCHWEDT 155

Table 1 Secondary Chronic Daily Headache patients suggest persistent activation of the trigemino- 16 Medication-overuse headache vascular system. Neurogenic inflammation may lead Cerebrovascular disease (cerebral venous sinus thrombosis, to central sensitization, a process implicated in the arteriovenous malformations, giant cell arteritis, subdural chronification of migraine. Functional and structural hematoma, etc.) brain changes have been identified in migraine and are Altered CSF dynamics (spontaneous CSF leak, idiopathic positively associated with increasing headache fre- 17 intracranial hypertension, secondary intracranial quency and duration. Chronic migraine sufferers hypertension) have increased iron deposition in the periaqueductal 18,19 Intracranial space-occupying lesions (neoplasms, others) gray, putamen, globus pallidus, and red nucleus. Posttraumatic They have reductions in gray and white matter density 20–22 Infection (intra- or extracranial, sinusitis) and volume in multiple regions of the brain. Musculoskeletal (cervical spine disorders, temporomandibular Migraine sufferers have inferior executive function joint disorders) andabnormalvisualmotionperceptionevenwhen 23,24 Others headache free. CSF, Cerebrospinal fluid. Diagnosis has. Chronic migraine, chronic tension-type headache, Chronic migraine patients tend to have mild to moder- new daily persistent headache, hemicrania continua, and ate headaches associated with mild migrainous features medication overuse headache are discussed in this re- (e.g., , phonophobia) with superimposed view. Although medication overuse headache is a sec- more-severe headaches associated with more prominent ondary CDH, it is included here because of the migraine features (‘‘full-blown’’ ). In some important contribution to primary CDH. patients, environmental hypersensitivities persist even during headache-free periods.25 This may include mild photophobia, phonophobia, motion-sensitivity, and cu- CHRONIC MIGRAINE taneous hypersensitivity/allodynia. Patients with chronic Chronic migraine, which affects 2% of the world migraine have an increased frequency of comorbid psy- population, places a substantial burden on individuals chiatric disorders, sleep disorders, fatigue, other pain, and societies.10 Chronic migraine results in poorer and gastrointestinal complaints. Recognition and treat- quality of life and causes significant disability.11,12 The ment of these comorbidities can result in improved World Health Organization considers chronic migraine health, greater quality of life, and may potentially result to cause disability on par with the disability secondary to in higher migraine treatment success rates. The follow- quadriplegia, dementia, and active psychosis.13 Direct ing are the recently revised diagnostic criteria for chronic and indirect costs from migraine are estimated at more migraine26: than $20 billion annually in the United States, much of which is due to chronic migraine.4 The average annual 1. Headache (tension-type and/or migraine) on 15 days cost per person with chronic migraine is more than four per month for at least 3 months times that associated with episodic migraine ($7750 2. Occurring in a patient who has had at least five attacks versus $1757).14 fulfilling criteria for migraine without aura Progression from episodic migraine (<15 head- 3. On 8 days per month for at least 3 months, headache ache days/month) to chronic migraine is referred to as has fulfilled criteria for pain and associated symptoms ‘‘transformed migraine.’’ In population studies, 3% of of migraine without aura (Criteria a and b below) or those with infrequent episodic headaches transform to was treated and relieved by triptan(s) or ergot before This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. CDH each year; 6% transform to frequent episodic the expected development of symptoms listed in headaches.1,15 In clinic-based studies, 14% of those Criteria a and b. with episodic migraine transform to chronic migraine a. Has at least two of the following: each year. Modifiable and nonmodifiable risk factors for i. Unilateral location this transformation have been described.15a ii. Pulsating quality A detailed discussion of migraine pathophysiol- iii. Moderate or severe pain intensity ogy is discussed in the article by Dr. Cutrer in this issue. iv. Aggravation by or causing avoidance of routine Interictal (between migraine) and longitudinal studies physical activity of chronic migraine will hopefully lead to an improved b. Has at least one of the following: understanding of the pathophysiology and effects of i. Nausea and/or vomiting transformation from episodic migraine to chronic mi- ii. Photophobia and phonophobia graine. Elevated concentrations of vasoactive neuro- 4. No medication overuse and not attributed to another peptides in the cerebrospinal fluid of chronic migraine causative disorder 156 SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 2 2010

Treatment Gabapentin Gabapentin has been studied as a pro- The treatment of chronic migraine focuses on prophy- phylactic medication for chronic daily headache in a lactic therapies, which may include avoidance of mi- multicenter randomized placebo-controlled crossover graine triggers, pharmacotherapy, physical therapy, study of 133 subjects (85% with migraine).29 Gaba- biobehavioral therapy, and others. Simultaneous use of pentin 2400 mg per day was associated with a greater these different therapeutic modalities may be needed. percentage of headache-free days (mean 26.6% Identification and treatment of comorbid disorders is vs. 17.5%, p < 0.001) and reductions in headache dura- also required for true treatment success. Acute headache tion, severity, and analgesic use. medication use needs to be limited to avoid medication overuse headache. Although complete headache eradi- Tizanidine Tizanidine has been studied as an adjunc- cation is not a realistic expectation, significant reductions tive prophylactic for chronic daily headache in a multi- in headache frequency and/or severity are the goal of center, randomized, blinded, placebo-controlled study.30 prophylactic therapy. One hundred thirty-six subjects (3/4 with chronic migraine) were randomized to placebo or to tizanidine PHARMACOLOGIC PROPHYLAXIS titrating up from 2 mg each night to the maximum Prophylactic medications used to treat episodic migraine tolerated dose, or 24 mg divided among three daily are also used for the prevention of chronic migraine. doses. The median tizanidine dosage was 20 mg per Thus, first-line prophylactic medications are from the day. Subjects in the tizanidine group had significant following classes: antidepressants, antiepileptics, and reductions in headache index as compared with the antihypertensives. The prophylactic medications that placebo group. have been specifically studied in clinical trials of patients with chronic migraine are illustrated in Table 2. Once an Fluoxetine Sixty-four subjects with chronic migraine effective prophylactic medication is found, it is typically were randomized in a 16-week double-blind trial of continued for 3 to 6 months prior to attempting dis- fluoxetine.31,32 Subjects were treated with 20 mg daily continuation. An effective prophylactic medication is and then increased to 40 mg daily if needed and as one that decreases headache frequency by at least 50%. tolerated. Fluoxetine-treated subjects had significant improvements as compared with the placebo group in Topiramate Two randomized, double-blind, placebo- overall headache status, mood, and headache frequency. controlled studies are available.27,28 The larger of the two studies randomized 153 subjects to topiramate 100 Amitriptyline Thirty-nine transformed migraine sub- mg daily and an equal number to placebo.27 Those in the jects participated in a prospective double-blind study of topiramate group experienced a reduction of 6.4 5.8 amitriptyline versus amitriptyline plus fluoxetine.32 headache days per month from a baseline of Although there were not significant differences in out- 17.1 5.4 days, as compared with a reduction of comes between the two treatment groups, subjects treated 4.7 6.1 days from a baseline of 17.0 5.0 days in the with amitriptyline (8–40 mg/day) and those treated with placebo group (p ¼ 0.10). In the smaller of the two amitriptyline plus fluoxetine (8–20 mg/day) both had studies, 32 subjects were randomized to topiramate reductions in headache frequency and intensity. 100 mg daily and 27 were randomized to placebo.28 Among all subjects, topiramate significantly reduced the Levetiracetam An open-label study of 36 transformed mean number of monthly migraine days during the third migraine subjects, with or without medication overuse, month of therapy as compared with placebo (p ¼ 0.02). investigated the effect of levetiracetam.33 At 3 months,

Table 2 Prophylactic Agents Studied Specifically in Chronic Migraine This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. Initial Dose Typical Total Drug (mg) Daily Dose (mg) Common Side Effects Serious Side Effects

Topiramate 25 100–200 Paresthesias, fatigue, weight loss Acute angle closure glaucoma, metabolic acidosis, hyperthermia Gabapentin 300 900–2400 Dizziness, somnolence, fatigue, edema Tizanidine 2 6–24 Somnolence, dry mouth, asthenia Hepatitis Fluoxetine 10–20 10–80 Insomnia, asthenia, tremor Prolonged QT interval Amitriptyline 10–25 50–150 Sedation, weight gain, constipation Cardiac dysrhythmias Levetiracetam 250 750–2000 Somnolence, asthenia Divalproex sodium 250–500 500–1500 Weight gain, tremor, nausea, alopecia Pancreatitis, liver failure, thrombocytopenia Memantine 5 5–20 Dizziness DIAGNOSIS AND MANAGEMENT OF CHRONIC DAILY HEADACHE/GARZA, SCHWEDT 157 levetiracetam-treated subjects had reductions in head- CHRONIC TENSION-TYPE HEADACHE ache frequency (24.9 days/month to 16.2 days/month; Chronic tension-type headache is considerably less prev- p < 0.001), disability (MIDAS dropped from 62.8 to alent than episodic tension-type headache.44 A tele- 40.8; p ¼ 0.01), and HIT-6 score (63.4 to 59.4; phone survey obtained from 1993 to 1994 in p 0.01). Baltimore, Maryland, found an overall prevalence of 38.3% for episodic tension-type headache and a 1-year Valproate Two studies suggest valproate may be useful period prevalence of chronic tension-type headache of in the prophylaxis of chronic migraine. In an open-label 2.2%.44 Chronic tension-type headache increases in study of 30 patients with intractable transformed mi- prevalence until the fourth decade of life and then graine, patients were maintained on dosages between decreases. Chronic tension-type headache is more prev- 1000 to 2500 mg.34 A 50% or greater reduction in alent in women compared with men and psychiatric headache index was found in 67% of the subjects, head- disorders may be risk factors for its development.44–48 ache-free days per month increased from 5.5 to 17.7, and Although peripheral mechanisms apparently play days with significant disability declined from 22 per a role in episodic tension-type headache pathophysiol- month to 8.5 per month. The second study was a chart ogy, central mechanisms may play a larger role in chronic review of 138 chronic daily headache patients (49 with tension-type headache.49,50 Chronic tension-type head- transformed migraine) being treated with divalproex ache sufferers had a general hypersensitivity to pain sodium monotherapy.35 In the migraine patients, the stimuli not seen in controls in a study of nociceptive mean decrease in migraine frequency was 65.2%. processing.51 Central pain inhibition may be dysfunc- tional in chronic tension-type headache. Research using Botulinum Toxin Although botulinum toxin type A high-density electroencephalogram (EEG) brain map- appears to benefit a subset of patients with chronic ping has found the supraspinal response to muscular pain migraine, no consistent or strong evidence is available to be abnormal in chronic tension-type headache suffer- yet to permit drawing conclusions on its efficacy in CDH ers.52 The reduced magnitude during and after induced (mainly transformed migraine).36 Further study results tonic muscle pain in controls, but not in chronic tension- are required and pending. type headache patients, might be a consequence of impaired inhibition of the nociceptive input in chronic Memantine Memantine was recently reported to in- tension-type headache.52 Deficient diffuse noxious in- duce remission of chronic migraine.37An open-label hibitory control-like mechanisms, such as seen in gen- study further suggests this drug may play a role in eralized chronic pain like fibromyalgia, have been found chronic migraine management.38 Double-blind studies in chronic tension-type headache.53 Voxel-based are required to establish memantine’s role in chronic morphometry and magnetic resonance imaging (MRI) migraine treatment. have identified a significant gray matter decrease in regions involved in pain processing in chronic tension- NONPHARMACOLOGIC THERAPY type headache patients.54 Biofeedback, relaxation therapy, cognitive–behavioral therapy, and physical therapy may be useful as adjunctive treatments for chronic migraine. A controlled study of Diagnosis biofeedback showed associated decreases in oxidative Because it largely consists of head pain alone, tension- stress and disability from migraine.39 Cognitive–behav- type headache is frequently called ‘‘the featureless head- ioral therapy may provide short-term and long-term ache.’’49 Chronic tension-type headache typically evolves reductions in headache burden.40 Physical therapy is from episodic tension-type headache55 and is usually associated with significant reductions in migraine bur- bilateral, pressure-like in quality, and mildly to moder- This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. den in some studies.41 Furthermore, a combination of ately intense. ‘‘Wearing a tight hat, wearing a tight band physical therapy and biofeedback has been shown to around the head, or wearing a heavy burden on the head’’ provide greater relief than physical therapy alone.42 are frequent descriptions used by patients.56 The follow- ing are current International Classification of Headache Disorders, 2nd edition (ICHD-2) criteria for chronic Outcome tension-type headache.55 Patients with chronic migraine may revert back to episodic migraine. Reversion rates at one year range 1. Headache occurring on 15 days per month on from 56 to 70% in population-based and specialty head- average for >3 months (180 days per year) and ache clinic-based samples, respectively.9,43 Predictors of fulfilling criteria 2–4 reversion include withdrawal of overused medications, 2. Headache lasts hours or may be continuous compliance with prophylactic medications, and regular 3. Headache has at least two of the following character- physical exercise. istics: 158 SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 2 2010

a. Bilateral location Protriptyline Twenty-five adult female chronic ten- b. Pressing/tightening (nonpulsating) quality sion-type headache sufferers were studied using protrip- c. Mild or moderate intensity tyline 20 mg every morning. Eighty-six percent had d. Not aggravated by routine physical activity such as fewer headaches per month, and 73% had a 50% walking or climbing stairs reduction in headache attacks per month.63 In contrast 4. Both of the following: to the weight gain associated with other tricyclic anti- a. No more than one of photophobia, phonophobia, or depressants, patients lost slightly over three pounds mild nausea during the study.63 No placebo group was used. b. Neither moderate or severe nausea nor vomiting 5. Not attributed to another disorder Mirtazapine Bendsten studied mirtazapine in a randomized, double-blind, placebo-controlled, crossover Of note, the presence of migraine attacks super- trial. Mirtazapine 15 to 30 mg/day or placebo was given imposed on a background daily ‘‘tension-type’’ headache for 8 weeks separated by a 2-week washout period.60 could suggest that chronic migraine may be the right Mirtazapine reduced the area-under-the-headache curve diagnosis rather than chronic tension-type headache.57 by 34% more than placebo. The drug also reduced headache frequency, duration, and intensity significantly more than placebo. The efficacy of mirtazapine was Treatment similar to that of amitriptyline (a therapeutic gain of Pharmacologic prophylaxis is the mainstay of treatment. 30%).59,60 Similar to chronic migraine, effective therapy is continued for at least 3 to 6 months prior to attempting discontin- Topiramate In an open study, topiramate (daily dose uation.58 Table 3 summarizes prophylactic medications 25 to 100 mg/day) resulted in a 50% reduction in studied specifically in chronic tension-type headache. headache frequency in 73% of 46 chronic tension-type headache patients at weeks 13 to 24.64 Average headache PHARMACOLOGIC PROPHYLAXIS intensity decreased from 6.13 to 2.07 on the visual analogue scale.64 Randomized controlled trials are Amitriptyline Amitriptyline is the drug of choice, needed to define topiramate’s role in the management typically at doses ranging from 25 mg to 100 mg per of chronic tension-type headache. day.50 This is the only antidepressant used in chronic tension-type headache that has demonstrated statisti- Sodium Valproate Sodium valproate (500 mg twice cally significant benefit in several trials.58 Amitriptyline per day) was associated with greater reductions in pain has an estimated therapeutic gain of 30% based on frequency than placebo in 41 chronic tension-type head- published trials.59,60 ache subjects in a prospective, double-blind, random- ized, placebo-controlled trial.65 The Visual Analog Scale Nortriptyline Nortriptyline has a more favorable side pain rating did not decrease in the active group. effect profile than amitriptyline.61 In a randomized placebo-controlled trial, patients with chronic tension- Tizanidine Tizanidine (6 to 18 mg/day in divided type headache who did not tolerate amitriptyline were doses) was found to be superior to placebo in a random- switched to nortriptyline at doses of up to 75 mg/day.62 ized, double-blind, crossover study in women with Both antidepressants produced larger reductions in chronic tension-type headache.66 A separate random- headache, analgesic medication use, and headache-re- ized, double-blind, parallel-group study, however, failed lated disability than placebo.62 to demonstrate superiority to placebo.67 To date, one This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited.

Table 3 Prophylactic Agents Studied in Chronic Tension-type Headache Initial Dose Typical Total Drug (mg) Daily Dose (mg) Common Side Effects Serious Side Effects

Amitriptyline 10–25 25–100 Sedation, weight gain, constipation Cardiac dysrhythmias Nortriptyline 10–25 25–100 Sedation, weight gain, constipation Cardiac dysrhythmias Protriptyline 5–10 10–30 Sedation, weight change, constipation Cardiac dysrhythmias Mirtazapine 15 15–45 Somnolence, dry mouth Neutropenia Topiramate 25 100–200 Paresthesias, fatigue, weight loss Acute angle closure glaucoma, metabolic acidosis, hyperthermia Sodium valproate 250–500 500–1000 Weight gain, tremor, nausea, alopecia Pancreatitis, liver failure, thrombocytopenia DIAGNOSIS AND MANAGEMENT OF CHRONIC DAILY HEADACHE/GARZA, SCHWEDT 159 cannot draw firm conclusions for the potential role of male ratio is 3.5:1.81 In tertiary headache clinics tizanidine in chronic tension-type headache.58 throughout America, up to 50 to 80% of patients have medication-overuse headache.80 By far, migraine is the Others Citalopram and paroxetine have not proven most common primary headache disorder associated beneficial in chronic tension-type headache prophy- with medication-overuse headache. In a meta-analysis laxis.59,68,69 Further research is needed to determine summarizing 29 studies, 65% of 2612 patients with the potential efficacy of venlafaxine70 and buspirone.71 chronic medication overuse headache had migraine, There is no evidence for a beneficial effect of botulinum 27% had tension-type, and 8% had mixed or other toxin in chronic tension-type headache.72 type of primary headache.81 The risk for medication overuse headache devel- COMPLEMENTARY/ALERNATIVE TREATMENT opment differs with individual substances. Opioids, In chronic tension-type headache sufferers with coex- butalbital-containing analgesics, and aspirin/acetamino- istent depression, simultaneous treatment for both dis- phen/caffeine combinations are high risk; triptans are orders has shown benefit.73 Combination treatment is moderate risk; and NSAIDs are low risk.82 In a recent superior to pharmacotherapy or behavioral therapy longitudinal population-based study, any use of barbi- alone.58 Combination treatment with behavioral stress turates and opiates was associated with increased risk of management was more likely to achieve clinically sig- transformed migraine.83 Critical dose of opiate exposure nificant (50%) reductions in headache index scores was around 8 days per month, and the effect was more (64% of participants) than antidepressant medication pronounced in men.84 Critical dose of barbiturate ex- (38% of participants), stress management therapy posure was around 5 days per month and the effect was (35%), or placebo (29%) in a randomized placebo-con- more pronounced in women.84 Triptans and NSAIDs trolled trial of 203 chronic tension-type headache sub- induced migraine progression in those with high fre- jects.62 quency of migraine at baseline (10–14 days per month), The potential role of acupuncture in chronic but not overall.84 tension-type headache is yet to be defined. In one study, Multiple mechanisms may be involved in the relaxation training induced the best benefit compared development of medication-overuse headache.85 Devel- with acupuncture and physical training.74 The potential opment of medication-overuse headache appears to be role of hypnosis75 and structured massage76 remain to be restricted to those with underlying headache disorders as determined. Other noninvasive physical treatments with it does not develop de novo in those without headaches some evidence in chronic tension-type headache pro- who overuse the same medications.85,86 Neurophysio- phylaxis include spinal manipulation, cranial electro- logic studies have shown facilitation of trigeminal and therapy, transcutaneous electrical nerve stimulation somatic nociceptive systems in medication-overuse head- (TENS)/electrical neurotransmitter modulation combi- ache, mainly mediated at a supraspinal level.87 This nation, and automassage/TENS/stretching combina- suggests central sensitization (a process also involved in tion.77 migraine pathophysiology) may also be involved in med- ication-overuse headache pathophysiology. Studies using ACUTE PHARMACOLOGIC THERAPY 18-fluorodeoxyglucose positron emission tomography Simple analgesics and nonsteroidal antiinflammatory (18-FDG PET) have identified reversible metabolic drugs (NSAIDs) remain as the pillar of abortive treat- changes in pain processing structures and persistent ment in tension-type headache.50 Acetaminophen/iso- orbitofrontal hypofunction in migraine patients with metheptene/ dichloralphenazone frequently helps more coexistent medication overuse headache.88 Chronic mor- severe episodes not responding to NSAIDs. phine exposure results in increased descending facilitation from the rostral88 ventromedial medulla and increased This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. excitatory neurotransmission at the dorsal horn.89 Some- MEDICATION-OVERUSE HEADACHE times, substance addiction may be the base for medication Medication-overuse headache frequently coexists with overuse headache. Others appear to be treating pain and a primary CDH and can preclude effective therapy of the comorbid anxiety disorder with the same medication latter. In some cases medication overuse headache may (e.g., opiates).90 Out of 895 patients with medication be responsible for the development or maintenance of a overuse headache studied in a prospective fashion, 68% CDH syndrome78; in other cases, medication overuse is met three of five substance-dependence criteria according the result of frequent headaches. Prophylactic medica- to the Diagnostic and Statistical Manual of Mental Dis- tions for primary CDH are more likely to provide benefit orders, Fourth Edition (DSM-IV ) versus 20% in those following successful medication-overuse headache man- without medication-overuse headache.91 Fear of head- agement.79 ache, anticipatory anxiety, obsessive drug-taking behav- The prevalence of medication-overuse headache iors, and psychological drug dependence may also help in the general population is 1.5%.80 The female to induce and then sustain medication-overuse headache.90 160 SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 2 2010

Diagnosis or from a ‘‘reparative’’ change from treatment failure to As discussed earlier, medication-overuse headache pa- favorable response to medical management.79,92 tients typically have a primary headache disorder that increased in frequency and led to increased analgesic consumption and then medication-overuse headache. It Withdrawal of the Offending Medication is not uncommon for patients to take frequent analgesics During analgesic withdrawal, headaches frequently ex- solely to prevent a severe analgesic-withdrawal head- acerbate before starting to improve.89 Nausea, vomiting, ache.85 Medication overuse headache varies in its char- restlessness, anxiety, and sleep disturbances may also acteristics (severity, location, type) and is frequently occur during withdrawal.85,89 Withdrawal symptoms associated with nausea, asthenia, and cognitive difficulties usually last 2 to 10 days (mean 3.5 days),85 but can (impaired memory, poor concentration, irritability).80 If a endure for 2 to 4 weeks.89 Although many physicians CDH sufferer is taking analgesics more than 2 to 3 days prefer inpatient programs for withdrawal,85 most pa- per week on average, medication-overuse headache tients can be managed on an outpatient basis.89 A recent should always be suspected. The following are current prospective, randomized trial in patients with migraine ICHD-2 diagnostic criteria for medication overuse head- and superimposed medication-overuse headache showed ache. Please note that the type of medication overused is that simple, strong advice was as effective as structured important for proper diagnosis.80 inpatient and outpatient detoxification programs in achieving medication withdrawal.93 The mean success 1. Headache present on 15 days/month rate of withdrawal treatment at 1 to 6 months was 72.4% 2. Regular overuse for >3 months of one or more acute/ in a meta-analysis.85 symptomatic treatment drugs a. Ergotamine, triptans, opioids, or combination an- algesic medications on 10 days/month on a reg- Bridging ular basis for >3 months Thegoalof‘‘bridging’’istoprovidesymptomaticrelief b. Simple analgesics or any combination of ergot- during acute medication withdrawal. No clear guide- amine, triptans, analgesic opioids on 15 days/ lines or consensus recommendations exist.94 Bridging month on a regular basis for >3 months without recommendations are based on case series, retrospective overuse of any single class alone chart reviews, prospective uncontrolled studies, and 3. Headache has developed or markedly worsened during expert opinion.89 Some studies support the use of medication overuse corticosteroids; others do not.95 Further randomized, placebo-controlled trials are needed to clarify the po- tential role of corticosteroids in medication-overuse Treatment headache management.96 Antiemetics are often pre- Abrupt drug withdrawal remains the treatment of choice scribed in addition to the following published strat- when dangerous physical withdrawal is not a concern.85 egies. Proper management of medication-overuse headache should include the following steps: ORAL Naproxen 500 mg twice a day until withdrawal is 1. Patient education complete97 2. Withdrawal of offending medication Naproxen sodium 550 mg twice a day for 2 to 4 weeks89 3. ‘‘Bridging’’ aimed at symptomatic relief during med- Naproxen sodium 550 mg twice a day for 1 week, then ication withdrawal once a day for 1 week89 4. Establish new acute and preventive headache treat- Prednisone 60 mg/day, decrease by 20 mg every 2 days This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. ment regimen (total 6 days)98 5. Follow-up and headache reassessment Prednisone 100 mg for 5 days96 6. Relapse prevention INJECTED Intravenous (IV) methylprednisolone 100 to 200 mg Patient Education every 12 hours for 2 to 3 days89,99 Patients with medication-overuse headache need to IV or intramuscular (IM) dexamethasone 8 to 20 mg/ understand that as long as they are overusing analgesics, day, tapering over 2 to 3 days98 headache preventives may be less effective or not effec- IV hydrocortisone 100 mg every 6 hours for 24 hours; tive at all.79,89 They need to be educated on why every 8 hours for 24 hours; then every 12 hours for analgesic overuse is detrimental. The majority of med- 24 hours98 ication-overuse headache patients benefit from drug Repetitive IV dihydroergotamine (DHE; inpatient): IV withdrawal. Benefit may be from the withdrawal alone metoclopramide 10 mg, followed by 0.5 mg IV DHE. DIAGNOSIS AND MANAGEMENT OF CHRONIC DAILY HEADACHE/GARZA, SCHWEDT 161

Doses adjusted based on headache severity and side headache affects women more than men with reported effects100 ratios of 1.3:1 and 2.5:1.0 and can essentially affect all Continuous IV DHE (inpatient): 3 mg of DHE in age groups.107–109 Peak age of onset is in the second and 1000 mL of normal saline at 42 mL/h by IV infusion third decades for women and the fifth decade in men.109 pump, totaling 3 mg of DHE administered at Overall mean age of onset is 35 years of age.108 Although constant rate over 24 hours101 new daily persistent headache is estimated to occur Subcutaneous DHE (outpatient): 1 mg twice a day for infrequently in the general population, the exact fre- 1 week followed by 0.5 mg twice a day for 1 week, or quency is unknown.108 In headache clinics, however, 1 mg twice a day for 1 week followed by 1 mg every 1 in 10 CDH patients have new daily persistent day for 1 week89 headache.110 IV valproate sodium: loading dose of 15 mg/kg followed The etiology of new daily persistent headache is by daily maintenance of 5 mg/kg every 8 hours for not well understood. Although the nature of the associ- 12 to 48 hours102 ations is unclear, infection, flu-like illness, surgery, and IV prochlorperazine starting with 5 mg to 10 mg every stressful life events may precede new daily persistent 8 hours, with dosage adjustment according to efficacy headache.109 How these may result in new daily persis- and side effects until headache-free99 tent headache is unknown and in many patients, no precipitating factors exist.108 Possible associations be- tween new daily persistent headache and Epstein-Barr Establish Appropriate Headache Prevention virus (EBV), herpes simplex virus (HSV), and cytome- Whether pharmacologic prophylaxis should be started at galovirus (CMV) have been suggested but remain the time of medication withdrawal remains an ongoing unproven.109,111–114 dispute.103 Because most patients will require long-term preventives, the authors recommend starting such treat- ment at the time of withdrawal. Preventives are chosen Diagnosis according to the type of underlying primary headache The vast majority of patients (up to 82%) can vividly disorder. recall the exact date the headache started.109 In most, 80%, the pain is continuous.108,109 Pain intensity tends to be moderate, although many patients experience Follow-up and Headache Reassessment severe pain.109 Clinical features vary significantly. Head- Once the overused medications have been withdrawn, aches may have primarily migraine features (photopho- patients frequently return to a pattern of intermittent bia, nausea, etc.) or be ‘‘featureless’’ and reminiscent of headaches. These headaches need to be classified and chronic tension-type headache.107–109 Secondary head- treated accordingly. ache disorders, including those due to spontaneous cerebrospinal (CSF) leaks and cerebral venous sinus thrombosis, need to be ruled out.55,106 MRI of the brain Relapse Prevention with gadolinium and magnetic resonance venography Most relapses occur in the first year following (MRV) should be considered. Clinical judgment guides withdrawal.104 In general, avoidance of opiates and/ further investigations, if any. Current ICHD-2 diag- or butalbital for the regular management of primary nostic criteria for new daily persistent headache are as headache disorders is recommended. Limitations follows:55 for the frequency of analgesic intake should be ex- plained: triptan or combination analgesic use should 1. Headache for >3monthsfulfillingCriteria2 be limited to 9 or fewer days a month on average and through 4 This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. NSAIDs to 15 or fewer days a month to prevent 2. Headache is daily and unremitting from onset or from medication-overuse headache relapse.105 The identi- <3 days from onset fication and management of comorbidities (anxiety, 3. At least two of the following pain characteristics: etc.) that may contribute to medication overuse head- a. Bilateral location ache development and preservation are of paramount b. Pressing/tightening (nonpulsating) quality importance to prevent medication overuse headache c. Mild or moderate intensity relapse.90 4. Not aggravated by routine physical activity, such as walking or climbing stairs 5. Both of the following: NEW DAILY PERSISTENT HEADACHE a. No more than one of photophobia, phonophobia, or New daily persistent headache, one of the most treat- mild nausea ment refractory headaches, is a headache that begins one b. Neither moderate or severe nausea nor vomiting day and typically does not remit.106 New daily persistent 6. Not attributed to another disorder 162 SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 2 2010

Of note, although the above criteria reflect essen- etc.).122 Although not fulfilling the diagnostic criteria,55 tially a chronic tension-type headache phenotype, mi- a subgroup of patients with continuous one-sided head- grainous features are frequently reported.115 Diagnostic aches completely responsive to indomethacin do not criteria will likely be modified as knowledge about this have autonomic symptoms.123 Mild migrainous features disorder expands. may be present, and some patients develop superimposed headaches consistent with migraine headaches.124 Ipsi- lateral ocular discomfort or an ocular foreign body Treatment sensation and a superimposed stabbing headache (‘‘jabs New daily persistent headache can endure for many years and jolts’’) are often reported.118 ICHD-2 diagnostic (even decades) and can be disabling. Despite proper criteria are as follows:55 treatment, the headache frequently does not abate.106 Takase found treatment to be very effective in 27%, 1. Headache for >3 months fulfilling Criteria 2 through moderately effective in 3%, mildly effective in 20%, and 4 not effective in 50% of 30 new daily persistent headache 2. All of the following characteristics: sufferers.108 In agreement with other headache special- a. Unilateral pain without side-shift ists,116 we recommend classifying the dominant head- b. Daily and continuous, without pain-free periods ache phenotype, whether it is migraine or tension-type, c. Moderate intensity, but with exacerbations of severe and treat with preventives accordingly. pain New daily persistent headache has been reported 3. At least one of the following autonomic features to take one of the following courses: a self-limited one occurs during exacerbations and ipsilateral to the typically resolving without treatment within several side of pain: months, or a refractory course resistant to aggressive a. Conjunctival injection and/or lacrimation treatment.55 Although most patients are headache free at b. Nasal congestion and/or 2 years in some series, in others (and in practice) new c. and/or daily persistent headache may be refractory to treatment 4. Complete response to therapeutic doses of indome- for many years.106–109,113 thacin 5. Not attributed to another disorder

HEMICRANIA CONTINUA Secondary headaches mimicking primary hemi- Hemicrania continua is a one-sided continuous head- crania continua (including response to indomethacin) ache of moderate severity with superimposed severe have been reported, including internal carotid artery exacerbations of pain often associated with ipsilateral dissection, unruptured aneurysm, pineal cyst, pituitary autonomic symptoms. The frequency of hemicrania tumor, ipsilateral mesenchymal tumor of the sphenoidal continua in the general population is unknown.117 bone involving the clinoid process at the base of the skull, Hemicrania continua may begin at any age, but peaks lung adenocarcinoma, and pontine stroke.125–130 Diag- in the third decade of life.118 It is twice as common in nostic studies must therefore be ordered as necessary. women than men.119 If hemicrania continua is suspected, an oral in- The pathophysiology of hemicrania continua is domethacin test can be used for the diagnosis of hemi- incompletely understood. However, a PET study of seven crania continua. One of several methods is as follows: patients with hemicrania continua showed significant 50 mg twice per day for 3 days, 50 mg three times per day activation of the contralateral posterior hypothalamus for 3 days, 50 mg four times per day for 3 days. and ipsilateral rostral pons during baseline pain that Indomethacin response is typically fast. In a prospective were blocked by administration of indomethacin.120 study of 12 hemicrania continua patients, complete pain This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. PET in one patient with hemicrania continua without relief was obtained within 48 hours in all cases, within autonomic features, who had dorsal pontine activation 24 hours in 10 of the patients, and within 8 hours in but no hypothalamic activation, suggests that the hypo- nine.131 Completion of the test without headache reso- thalamus may play a role in autonomic activation, perhaps lution is considered a failed trial. via disinhibition of the trigeminal-autonomic reflex.121

Treatment Diagnosis Due to absolute response to indomethacin, it is the Hemicrania continua is a unilateral headache that is treatment of choice for hemicrania continua. The ap- continuous in nature. Continuous pain is generally propriate dose will vary among patients. The initial dose moderate in intensity. There are superimposed severe is that dose which results in resolution of headache, attacks of pain that last minutes to several days classically determined during the diagnostic indomethacin trial. associated with autonomic features (lacrimation, miosis, Oral doses ranging from 25 mg to 300 mg per day DIAGNOSIS AND MANAGEMENT OF CHRONIC DAILY HEADACHE/GARZA, SCHWEDT 163 have been reported effective. However, given adverse population, and dependency ratios. Bull World Health side effects of indomethacin, the lowest effective dose is Organ 2004;82(4):251–258 the desired dose. Periodic attempts to decrease the dose 14. Munakata J, Hazard E, Serrano D, et al. Economic burden should be made. Potential side effects from indometha- of transformed migraine: results from the American Migraine Prevalence and Prevention (AMPP) Study. Head- cin are numerous. Administration of indomethacin with ache 2009;49(4):498–508 food can reduce gastrointestinal side effects. Treatment 15. Katsarava Z, Schneeweiss S, Kurth T, et al. Incidence and with gastric mucosal protectants, such as proton-pump predictors for chronicity of headache in patients with inhibitors, may also decrease this risk and is common episodic migraine. Neurology 2004;62(5):788–790 practice. Many of these potential side effects are dose- 15a. Lipton RB. Tracing transformation: chronic migration related. Approximately one of three patients report side classification, progression, and epidemiology. Neurology effects attributable to indomethacin therapy.132 Contra- 2009;72(5 Suppl):S3–S7 16. Sarchielli P, Alberti A, Floridi A, Gallai V. Levels of nerve indications to treatment with indomethacin and/or growth factor in cerebrospinal fluid of chronic daily discontinuation due to intolerance have led to the search headache patients. Neurology 2001;57(1):132–134 for alternative therapies. There have been case reports 17. Schwedt TJ, Dodick DW. Advanced neuroimaging of of efficacy with melatonin, topiramate, verapamil, cox-2 migraine. Lancet Neurol 2009;8(6):560–568 inhibitors, gabapentin, botulinum toxin type A, and 18. Welch KM, Nagesh V, Aurora SK, Gelman N. Periaque- occipital nerve stimulation.119,133–138 ductal gray matter dysfunction in migraine: cause or the burden of illness? Headache 2001;41(7):629–637 19. Kruit MC, Launer LJ, Overbosch J, van Buchem MA, Ferrari MD. Iron accumulation in deep brain nuclei in REFERENCES migraine: a population-based magnetic resonance imaging study. Cephalalgia 2009;29(3):351–359 1. Scher AI, Stewart WF, Liberman J, Lipton RB. Prevalence 20. Schmitz N, Admiraal-Behloul F, Arkink EB, et al. Attack of frequent headache in a population sample. Headache frequency and disease duration as indicators for brain 1998;38(7):497–506 damage in migraine. Headache 2008;48(7):1044–1055 2. Lu SR, Fuh JL, Chen WT, Juang KD, Wang SJ. Chronic 21. Valfre` W, Rainero I, Bergui M, Pinessi L. Voxel-based daily headache in Taipei, Taiwan: prevalence, follow-up and morphometry reveals gray matter abnormalities in migraine. outcome predictors. Cephalalgia 2001;21(10):980–986 Headache 2008;48(1):109–117 3. Wang SJ, Fuh JL, Lu SR, et al. Chronic daily headache in 22. Rocca MA, Ceccarelli A, Falini A, et al. Brain gray matter Chinese elderly: prevalence, risk factors, and biannual changes in migraine patients with T2-visible lesions: a 3-T follow-up. Neurology 2000;54(2):314–319 MRI study. Stroke 2006;37(7):1765–1770 4. Stewart WF, Ricci JA, Chee E, Morganstein D, Lipton R. 23. Schmitz N, Arkink EB, Mulder M, et al. Frontal lobe Lost productive time and cost due to common pain conditions structure and executive function in migraine patients. in the US workforce. JAMA 2003;290(18):2443–2454 Neurosci Lett 2008;440(2):92–96 5. Lipton RB, Stewart WF, Scher AI. Epidemiology and 24. Granziera C, DaSilva AF, Snyder J, Tuch DS, Hadjikhani economic impact of migraine. Curr Med Res Opin 2001;17 N. Anatomical alterations of the visual motion processing (Suppl 1):s4–s12 network in migraine with and without aura. PLoS Med 6. Scher AI, Midgette LA, Lipton RB. Risk factors for 2006;3(10):e402 headache chronification. Headache 2008;48(1):16–25 25. Ashkenazi A, Mushtaq A, Yang I, Oshinsky ML. Ictal and 7. Scher AI, Stewart WF, Buse D, Krantz DS, Lipton RB. interictal phonophobia in migraine-a quantitative controlled Major life changes before and after the onset of chronic daily study. Cephalalgia 2009;29(10):1042–1048 headache: a population-based study. Cephalalgia 2008;28 26. Olesen J, Bousser MG, Diener HC, et al; Headache (8):868–876 Classification Committee. New appendix criteria open for a 8. Scher AI, Stewart WF, Lipton RB. Caffeine as a risk factor broader concept of chronic migraine. Cephalalgia 2006; for chronic daily headache: a population-based study. 26(6):742–746 Neurology 2004;63(11):2022–2027 27. Silberstein SD, Lipton RB, Dodick DW, et al; Topiramate 9. Scher AI, Stewart WF, Ricci JA, Lipton RB. Factors Chronic Migraine Study Group. Efficacy and safety of This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. associated with the onset and remission of chronic daily topiramate for the treatment of chronic migraine: a headache in a population-based study. Pain 2003;106(1-2): randomized, double-blind, placebo-controlled trial. Head- 81–89 ache 2007;47(2):170–180 10. Castillo J, Mun˜oz P, Guitera V, Pascual J. Kaplan Award 28. Diener HC, Bussone G, Van Oene JC, Lahaye M, 1998. Epidemiology of chronic daily headache in the general Schwalen S, Goadsby PJ; TOPMAT-MIG-201(TOP- population. Headache 1999;39(3):190–196 CHROME) Study Group. Topiramate reduces headache 11. Guitera V, Mun˜oz P, Castillo J, Pascual J. Quality of life in days in chronic migraine: a randomized, double-blind, chronic daily headache: a study in a general population. placebo-controlled study. Cephalalgia 2007;27(7):814–823 Neurology 2002;58(7):1062–1065 29. Spira PJ, Beran R; GAustralian Gabapentin Chronic Daily 12. D’Amico D, Usai S, Grazzi L, et al. Quality of life and Headache Group. Gabapentin in the prophylaxis of chronic disability in primary chronic daily headaches. Neurol Sci daily headache: a randomized, placebo-controlled study. 2003;24(Suppl 2):S97–S100 Neurology 2003;61(12):1753–1759 13. Harwood RH, Sayer AA, Hirschfeld M. Current and future 30. Saper JR, Lake AE III, Cantrell DT, Winner PK, White worldwide prevalence of dependency, its relationship to total JR. Chronic daily headache prophylaxis with tizanidine: 164 SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 2 2010

a double-blind, placebo-controlled, multicenter outcome 49. Fumal AS. Chronic tension-type headache. In: Goadsby PJ, study. Headache 2002;42(6):470–482 Dodick DW, eds. Chronic Daily Headache for Clinicians. 31. Saper JR, Silberstein SD, Lake AE III, Winters ME. 1st Ed. Hamilton, Ontario: BC Decker Inc; 2005:57–64 Double-blind trial of fluoxetine: chronic daily headache and 50. Mathew NT. Tension-type headache. Curr Neurol Neuro- migraine. Headache 1994;34(9):497–502 sci Rep 2006;6(2):100–105 32. Krymchantowski AV, Silva MT, Barbosa JS, Alves LA. 51. Bendtsen L, Jensen R, Olesen J. Decreased pain detection Amitriptyline versus amitriptyline combined with fluoxetine and tolerance thresholds in chronic tension-type headache. in the preventative treatment of transformed migraine: a Arch Neurol 1996;53(4):373–376 double-blind study. Headache 2002;42(6):510–514 52. Buchgreitz L, Egsgaard LL, Jensen R, Arendt-Nielsen L, 33. Rapoport AM, Sheftell FD, Tepper SJ, Bigal M. Levetir- Bendtsen L. Abnormal pain processing in chronic tension- acetam in the preventive treatment of transformed migraine. type headache: a high-density EEG brain mapping study. Curr Ther Res 2005;66:212–221 Brain 2008;131(Pt 12):3232–3238 34. Mathew NT, Ali S. Valproate in the treatment of persistent 53. Pielsticker A, Haag G, Zaudig M, Lautenbacher S. chronic daily headache. An open label study. Headache 1991; Impairment of pain inhibition in chronic tension-type 31(2):71–74 headache. Pain 2005;118(1-2):215–223 35. Freitag FG, Diamond S, Diamond ML, Urban GJ. 54. Schmidt-Wilcke T, Leinisch E, Straube A, et al. Gray Divalproex in the long-term treatment of chronic daily matter decrease in patients with chronic tension type headache. Headache 2001;41(3):271–278 headache. Neurology 2005;65(9):1483–1486 36. Naumann M, So Y, Argoff CE, et al; Therapeutics and 55. Headache Classification Subcommittee of the International Technology Assessment Subcommittee of the American Headache Society. The International Classification of Academy of Neurology. Assessment: Botulinum neurotoxin Headache Disorders, 2nd Edition. Cephalalgia 2004; in the treatment of autonomic disorders and pain (an 24(Suppl 1):1–160 evidence-based review): report of the Therapeutics and 56. Jensen R, Becker WJ. Symptomatology of chronic tension- Technology Assessment Subcommittee of the American type headaches. In: Olesen J, Ramadan NM, Tfelt-Hansen Academy of Neurology. Neurology 2008;70(19):1707–1714 P, Welch KMA, eds. The Headaches. 3rd ed. Philadelphia: 37. Spengos K, Theleritis C, Paparrigopoulos T. Memantine Lippincott Williams and Wilkins; 2006:693–699 and NMDA antagonism for chronic migraine: a potentially 57. Bigal ME, Lipton RB. Tension-type headache: classifica- novel therapeutic approach? Headache 2008;48(2):284–286 tion and diagnosis. Curr Pain Headache Rep 2005;9(6): 38. Bigal M, Rapoport A, Sheftell F, Tepper D, Tepper S. 423–429 Memantine in the preventive treatment of refractory 58. Lenaerts ME. Pharmacoprophylaxis of tension-type head- migraine. Headache 2008;48(9):1337–1342 ache. Curr Pain Headache Rep 2005;9(6):442–447 39. Ciancarelli I, Tozzi-Ciancarelli MG, Spacca G, Di 59. Bendtsen L, Jensen R, Olesen J. A non-selective (amitripty- Massimo C, Carolei A. Relationship between biofeedback line), but not a selective (citalopram), serotonin reuptake and oxidative stress in patients with chronic migraine. inhibitor is effective in the prophylactic treatment of chronic Cephalalgia 2007;27(10):1136–1141 tension-type headache. J Neurol Neurosurg Psychiatry 1996; 40. Martin PR, Forsyth MR, Reece J. Cognitive-behavioral 61(3):285–290 therapy versus temporal pulse amplitude biofeedback train- 60. Bendtsen L, Jensen R. Mirtazapine is effective in the ing for recurrent headache. Behav Ther 2007;38(4):350–363 prophylactic treatment of chronic tension-type headache. 41. Lockett DM, Campbell JF. The effects of aerobic exercise Neurology 2004;62(10):1706–1711 on migraine. Headache 1992;32(1):50–54 61. Garza I, Swanson JW. Prophylaxis of migraine. Neuro- 42. Marcus DA, Scharff L, Mercer S, Turk DC. Non- psychiatr Dis Treat 2006;2(3):281–291 pharmacological treatment for migraine: incremental utility 62. Holroyd KA, O’Donnell FJ, Stensland M, Lipchik GL, of physical therapy with relaxation and thermal biofeedback. Cordingley GE, Carlson BW. Management of chronic Cephalalgia 1998;18(5):266–272, discussion 242 tension-type headache with tricyclic antidepressant medi- 43. Seok JI, Cho HI, Chung CS. From transformed migraine to cation, stress management therapy, and their combination: a episodic migraine: reversion factors. Headache 2006;46(7): randomized controlled trial. JAMA 2001;285(17):2208– 1186–1190 2215 44. Schwartz BS, Stewart WF, Simon D, Lipton RB. 63. Cohen GL. Protriptyline, chronic tension-type headaches, Epidemiology of tension-type headache. JAMA 1998; and weight loss in women. Headache 1997;37(7):433–436 This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. 279(5):381–383 64. Lampl C, Marecek S, May A, Bendtsen L. A prospective, 45. Lavados PM, Tenhamm E. Epidemiology of tension-type open-label, long-term study of the efficacy and tolerability headache in Santiago, Chile: a prevalence study. Cephalalgia of topiramate in the prophylaxis of chronic tension-type 1998;18(8):552–558 headache. Cephalalgia 2006;26(10):1203–1208 46. Russell MB, Levi N, Saltyte-Benth J, Fenger K. Tension- 65. Yurekli VA, Akhan G, Kutluhan S, Uzar E, Koyuncuoglu type headache in adolescents and adults: a population based HR, Gultekin F. The effect of sodium valproate on chronic study of 33,764 twins. Eur J Epidemiol 2006;21(2):153– daily headache and its subgroups. J Headache Pain 2008; 160 9(1):37–41 47. Bendtsen L, Jensen R. Tension-type headache: the most 66. Fogelholm R, Murros K. Tizanidine in chronic tension-type common, but also the most neglected, headache disorder. headache: a placebo controlled double-blind cross-over Curr Opin Neurol 2006;19(3):305–309 study. Headache 1992;32(10):509–513 48. Juang KD, Wang SJ, Fuh JL, Lu SR, Su TP. Comorbidity 67. Murros K, Kataja M, Hedman C, et al. Modified-release of depressive and anxiety disorders in chronic daily headache formulation of tizanidine in chronic tension-type headache. and its subtypes. Headache 2000;40(10):818–823 Headache 2000;40(8):633–637 DIAGNOSIS AND MANAGEMENT OF CHRONIC DAILY HEADACHE/GARZA, SCHWEDT 165

68. Langemark M, Olesen J. Sulpiride and paroxetine in the 87. Ayzenberg I, Obermann M, Nyhuis P, et al. Central treatment of chronic tension-type headache. An explanatory sensitization of the trigeminal and somatic nociceptive double-blind trial. Headache 1994;34(1):20–24 systems in medication overuse headache mainly involves 69. Holroyd KA, Labus JS, O’Donnell FJ, Cordingley GE. cerebral supraspinal structures. Cephalalgia 2006;26(9): Treating chronic tension-type headache not responding to 1106–1114 amitriptyline hydrochloride with paroxetine hydrochloride: 88. Fumal A, Laureys S, Di Clemente L, et al. Orbitofrontal a pilot evaluation. Headache 2003;43(9):999–1004 cortex involvement in chronic analgesic-overuse headache 70. Adelman LC, Adelman JU, Von Seggern R, Mannix LK. evolving from episodic migraine. Brain 2006;129(Pt 2):543– Venlafaxine extended release (XR) for the prophylaxis of 550 migraine and tension-type headache: A retrospective study 89. Boes CJ, Black DF, Dodick DW. Pathophysiology and in a clinical setting. Headache 2000;40(7):572–580 management of transformed migraine and medication 71. Mitsikostas DD, Gatzonis S, Thomas A, Ilias A. Buspirone overuse headache. Semin Neurol 2006;26(2):232–241 vs amitriptyline in the treatment of chronic tension-type 90. Saper JR, Hamel RL, Lake AE III. Medication overuse headache. Acta Neurol Scand 1997;96(4):247–251 headache (MOH) is a biobehavioural disorder. Cephalalgia 72. Schulte-Mattler WJ, Martinez-Castrillo JC. Botulinum toxin 2005;25(7):545–546 therapy of migraine and tension-type headache: comparing 91. Fuh JL, Wang SJ, Lu SR, Juang KD. Does medication different botulinum toxin preparations. Eur J Neurol 2006; overuse headache represent a behavior of dependence? Pain 13(Suppl 1):51–54 2005;119(1-3):49–55 73. Walker Z, Walker RW, Robertson MM, Stansfeld S. 92. Zeeberg P, Olesen J, Jensen R. Discontinuation of Antidepressant treatment of chronic tension-type headache: medication overuse in headache patients: recovery of a comparison between fluoxetine and desipramine. Head- therapeutic responsiveness. Cephalalgia 2006;26(10):1192– ache 1998;38(7):523–528 1198 74. So¨derberg E, Carlsson J, Stener-Victorin E. Chronic 93. Rossi P, Di Lorenzo C, Faroni J, Cesarino F, Nappi G. tension-type headache treated with acupuncture, physical Advice alone vs. structured detoxification programmes for training and relaxation training. Between-group differences. medication overuse headache: a prospective, randomized, Cephalalgia 2006;26(11):1320–1329 open-label trial in transformed migraine patients with low 75. Melis PM, Rooimans W, Spierings EL, Hoogduin CA. medical needs. Cephalalgia 2006;26(9):1097–1105 Treatment of chronic tension-type headache with hypno- 94. Obermann M, Katsarava Z. Management of medication- therapy: a single-blind time controlled study. Headache overuse headache. Expert Rev Neurother 2007;7(9): 1991;31(10):686–689 1145–1155 76. Quinn C, Chandler C, Moraska A. Massage therapy and 95. Bøe MG, Mygland A, Salvesen R. Prednisolone does not frequency of chronic tension headaches. Am J Public Health reduce withdrawal headache: a randomized, double-blind 2002;92(10):1657–1661 study. Neurology 2007;69(1):26–31 77. Bronfort G, Nilsson N, Haas M, et al. Non-invasive physical 96. Diener HC. How to treat medication-overuse headache: treatments for chronic/recurrent headache. Cochrane Data- prednisolone or no prednisolone? Neurology 2007;69(1): base Syst Rev 2004;(3):CD001878 14–15 78. Bigal ME, Rapoport AM, Sheftell FD, Tepper SJ, Lipton 97. Mathew NT. Amelioration of ergotamine withdrawal RB. Transformed migraine and medication overuse in a symptoms with naproxen. Headache 1987;27(3):130–133 tertiary headache centre—clinical characteristics and treat- 98. Krymchantowski AV, Barbosa JS. Prednisone as initial ment outcomes. Cephalalgia 2004;24(6):483–490 treatment of analgesic-induced daily headache. Cephalalgia 79. Mathew NT, Kurman R, Perez F. Drug induced refractory 2000;20(2):107–113 headache—clinical features and management. Headache 99. Lu SR, Fuh JL, Juang KD, Wang SJ. Repetitive intra- 1990;30(10):634–638 venous prochlorperazine treatment of patients with 80. Dodick D, Freitag F. Evidence-based understanding of refractory chronic daily headache. Headache 2000;40(9): medication-overuse headache: clinical implications. Head- 724–729 ache 2006;46(Suppl 4):S202–S211 100. Silberstein SD, Schulman EA, Hopkins MM. Repetitive 81. Kavuk I, Katsarava Z, Selekler M, et al. Clinical features and intravenous DHE in the treatment of refractory headache. therapy of medication overuse headache. Eur J Med Res Headache 1990;30(6):334–339 2004;9(12):565–569 101. Ford RG, Ford KT. Continuous intravenous dihydroergot- This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. 82. Smith TR, Stoneman J. Medication overuse headache from amine in the treatment of intractable headache. Headache antimigraine therapy: clinical features, pathogenesis and 1997;37(3):129–136 management. Drugs 2004;64(22):2503–2514 102. Schwartz TH, Karpitskiy VV, Sohn RS. Intravenous 83. Bigal ME, Serrano D, Buse D, Scher A, Stewart WF, valproate sodium in the treatment of daily headache. Lipton RB. Acute migraine medications and evolution from Headache 2002;42(6):519–522 episodic to chronic migraine: a longitudinal population- 103. Katsarava Z, Jensen R. Medication-overuse headache: where based study. Headache 2008;48(8):1157–1168 are we now? Curr Opin Neurol 2007;20(3):326–330 84. Bigal ME, Lipton RB. Excessive acute migraine medication 104. Katsarava Z, Muessig M, Dzagnidze A, Fritsche G, Diener use and migraine progression. Neurology 2008;71(22):1821– HC, Limmroth V. Medication overuse headache: rates and 1828 predictors for relapse in a 4-year prospective study. 85. Diener HC, Limmroth V. Medication-overuse headache: a Cephalalgia 2005;25(1):12–15 worldwide problem. Lancet Neurol 2004;3(8):475–483 105. Garza I, Swanson JW. Answers to frequently asked questions 86. Lance F, Parkes C, Wilkinson M. Does analgesic abuse about migraine. Mayo Clin Proc 2006;81(10):1387–1391, cause headaches de novo? Headache 1988;28(1):61–62 quiz 1392 166 SEMINARS IN NEUROLOGY/VOLUME 30, NUMBER 2 2010

106. Rozen TD. New daily persistent headache. Curr Pain 123. Marmura MJ, Silberstein SD, Gupta M. Hemicrania Headache Rep 2003;7(3):218–223 continua: who responds to indomethacin? Cephalalgia 2009; 107. Vanast WJ. New daily persistent headaches definition of a 29(3):300–307 benign syndrome. Headache 1986;26:317–320 (Abstract) 124. Bigal ME, Tepper SJ, Rapoport AM, Sheftell FD. Hemi- 108. Takase Y, Nakano M, Tatsumi C, Matsuyama T. Clinical crania continua: comparison between two different classi- features, effectiveness of drug-based treatment, and prog- fication systems. Cephalalgia 2002;22(3):242–245 nosis of new daily persistent headache (NDPH): 30 cases in 125. Eross EJ, Swanson JW, Dodick DW. Hemicrania continua: Japan. Cephalalgia 2004;24(11):955–959 an indomethacin-responsive case with an underlying 109. Li D, Rozen TD. The clinical characteristics of new daily malignant etiology. Headache 2002;42(6):527–529 persistent headache. Cephalalgia 2002;22(1):66–69 126. Antonaci F, Sjaastad O. Hemicrania continua: a possible 110. Bigal ME, Sheftell FD, Rapoport AM, Lipton RB, Tepper symptomatic case, due to mesenchymal tumor. Funct Neurol SJ. Chronic daily headache in a tertiary care population: 1992;7(6):471–474 correlation between the International Headache Society 127. Valenc¸a MM, Andrade-Valenc¸a LP, da Silva WF, Dodick diagnostic criteria and proposed revisions of criteria for DW. Hemicrania continua secondary to an ipsilateral chronic daily headache. Cephalalgia 2002;22(6):432–438 brainstem lesion. Headache 2007;47(3):438–441 111. Diaz-Mitoma F, Vanast WJ, Tyrrell DL. Increased 128. Rogalewski A, Evers S. Symptomatic hemicrania continua frequency of Epstein-Barr virus excretion in patients with after internal carotid artery dissection. Headache 2005;45(2): new daily persistent headaches. Lancet 1987;1(8530):411– 167–169 415 129. Peres MF, Zukerman E, Porto PP, Brandt RA. Headaches 112. Hamada T, Ohshima K, Ide Y, Sakato S, Takamori M. A and pineal cyst: a (more than) coincidental relationship? case of new daily persistent headache with elevated antibodies Headache 2004;44(9):929–930 to Epstein-Barr virus. Jpn J Med 1991;30(2):161–163 130. Levy MJ, Matharu MS, Meeran K, Powell M, Goadsby PJ. 113. Meineri P, Torre E, Rota E, Grasso E. New daily persistent The clinical characteristics of headache in patients with headache: clinical and serological characteristics in a retro- pituitary tumours. Brain 2005;128(Pt 8):1921–1930 spective study. Neurol Sci 2004;25(Suppl 3):S281–S282 131. Pareja J, Sjaastad O. Chronic paroxysmal hemicrania and 114. Santoni JR, Santoni-Williams CJ. Headache and painful hemicrania continua. Interval between indomethacin lymphadenopathy in extracranial or systemic infection: administration and response. Headache 1996;36(1):20–23 etiology of new daily persistent headaches. Intern Med 132. Pareja JA, Caminero AB, Franco E, Casado JL, Pascual J, 1993;32(7):530–532 Sa´nchez del Rı´o M. Dose, efficacy and tolerability of long- 115. Rozen TD. New daily persistent headache. In: Goadsby PJ, term indomethacin treatment of chronic paroxysmal hemi- Dodick DW, eds. Chronic Daily Headache for Clinicians. crania and hemicrania continua. Cephalalgia 2001;21(9):906– 1st Ed. Hamilton, Ontario: BC Decker Inc.; 2005:209–215 910 116. Goadsby PJ, Boes C. New daily persistent headache. 133. Rozen TD. Melatonin responsive hemicrania continua. J Neurol Neurosurg Psychiatry 2002;72(Suppl 2):ii6–ii9 Headache 2006;46(7):1203–1204 117. Rossi P, Faroni J, Tassorelli C, Nappi G. Diagnostic delay 134. Peres MF, Silberstein SD. Hemicrania continua responds to and suboptimal management in a referral population with cyclooxygenase-2 inhibitors. Headache 2002;42(6):530–531 hemicrania continua. Headache 2009;49(2):227–234 135. Schwedt TJ, Dodick DW, Hentz J, Trentman TL, 118. Peres MF, Silberstein SD, Nahmias S, et al. Hemicrania Zimmerman RS. Occipital nerve stimulation for chronic continua is not that rare. Neurology 2001;57(6):948–951 headache—long-term safety and efficacy. Cephalalgia 119. Dodick D. Hemicrania continua: diagnostic criteria and 2007;27(2):153–157 nosologic status. Cephalalgia 2001;21(9):869–872 136. Camarda C, Camarda R, Monastero R. Chronic paroxysmal 120. Matharu MS, Cohen AS, McGonigle DJ, Ward N, hemicrania and hemicrania continua responding to top- Frackowiak RS, Goadsby PJ. Posterior hypothalamic and iramate: two case reports. Clin Neurol Neurosurg 2008; brainstem activation in hemicrania continua. Headache 110(1):88–91 2004;44(8):747–761 137. Burns B, Watkins L, Goadsby PJ. Treatment of hemicrania 121. Irimia P, Arbizu J, Prieto E, Ferna´ndez-Torro´nR, continua by occipital nerve stimulation with a bion device: Martı´nez-Vila E. Activation of the brainstem but not of long-term follow-up of a crossover study. Lancet Neurol the hypothalamus in hemicrania continua without auto- 2008;7(11):1001–1012 nomic symptoms. Cephalalgia 2009;29(9):974–979 138. Garza I, Cutrer F. Pain relief and persistence of dysanto- This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited. 122. Matharu MS, Boes CJ, Goadsby PJ. Management of nomic features in a patient with hemicrania continua trigeminal autonomic cephalgias and hemicrania continua. responsive to botulinum toxin type A. Cephalalgia 2009; Drugs 2003;63(16):1637–1677 June 10 (Epub ahead of print)